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A cure for Type 1 diabetes is a step closer after scientists managed to halt the condition for at least six months thanks to insulin-producing cells.

Experts from U.S. hospitals and institutions including Harvard University managed to transplant cells into mice, which immediately began producing insulin.

The team was also able to show they could prevent the cells being rendered useless by the body’s own immune system, which was effectively ‘switched off’ thanks to scientific work.

It means a cure for Type 1 diabetes – which affects 400,000 people in the UK – could be much closer.

Scientists are now working to replicate the results in people with the condition.

The findings build on the news at the end of 2014 that experts had discovered how to make huge quantities of insulin-producing cells.

The man who led that breakthrough – Harvard professor Doug Melton who has been trying to find a cure for the disease since his son Sam was diagnosed with Type 1 diabetes as a baby – also worked on the new studies.

The human islet cells used for the new research were generated from human stem cells developed by Professor Melton.

Following implantation in mice, the cells immediately began producing insulin in response to blood glucose levels and were able to maintain blood glucose within a healthy range for 174 days – the length of the study.

The findings are published in the journals Nature Medicine and Nature Biotechnology and were made possible with funding from the Juvenile Diabetes Research Foundation (JDRF).

In one study, experts were able to create a newly-modified alginate material to encapsulate human pancreatic islet cells – a way of making the body adopt them.

The modified alginate, a material originally derived from brown algae, was used to prevent the body triggering an immune response which can lead to the build-up of scar tissue and the cells ultimately being rendered useless.

Scientists created a library of almost 800 alginate derivatives and evaluated the immune response to each of them.

This led them to focus on one called triazole-thiomorpholine dioxide (TMTD), which had a minimal immune response in mice and large animals.

The researchers then implanted human islet cells encapsulated in TMTD in mice, which provided the success for the study.

JDRF’s vice president of discovery research, Julia Greenstein, said: ‘Encapsulation therapies have the potential to be groundbreaking for people with Type 1 diabetes.

‘These treatments aim to effectively establish long-term insulin independence and eliminate the daily burden of managing the disease for months, possibly years, at a time without the need for immune suppression.

‘JDRF is excited by these findings and we hope to see this research progress into human clinical trials and ultimately a potential new Type 1 diabetes therapy.’

Senior author of the research, Daniel Anderson, who is associate professor at the Massachusetts Institute of Technology’s department of chemical engineering, said: ‘We are excited by these results, and are working hard to advance this technology to the clinic.’

Scientists at the Salk Institute have discovered an on-and-off “switch” in cells that may hold the key to healthy aging. This switch points to a way to encourage healthy cells to keep dividing and generating, for example, new lung or liver tissue, even in old age.

In our bodies, newly divided cells constantly replenish lungs, skin, liver and other organs. However, most human cells cannot divide indefinitely – with each division, a cellular timekeeper at the ends of chromosomes shortens. When this timekeeper, called a telomere, becomes too short, cells can no longer divide, causing organs and tissues to degenerate, as often happens in old age. But there is a way around this countdown: some cells produce an enzyme called telomerase, which rebuilds telomeres and allows cells to divide indefinitely.

In a new study published September 19th in the journal Genes and Development, scientists at the Salk Institute have discovered that telomerase, even when present, can be turned off.

.……………………….Victoria Lundblad and Timothy Tucey

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“Previous studies had suggested that once assembled, telomerase is available whenever it is needed,” says senior author Vicki Lundblad, professor and holder of Salk’s Ralph S. and Becky O’Connor Chair. “We were surprised to discover instead that telomerase has what is in essence an ‘off’ switch, whereby it disassembles.”

Understanding how this “off” switch can be manipulated – thereby slowing down the telomere shortening process – could lead to treatments for diseases of aging (for example, regenerating vital organs later in life).

Lundblad and first author and graduate student Timothy Tucey conducted their studies in the yeast Saccharomyces cerevisiae, the same yeast used to make wine and bread. Previously, Lundblad’s group used this simple single-celled organism to reveal numerous insights about telomerase and lay the groundwork for guiding similar findings in human cells.

“We wanted to be able to study each component of the telomerase complex but that turned out to not be a simple task,” Tucey said. Tucey developed a strategy that allowed him to observe each component during cell growth and division at very high resolution, leading to an unanticipated set of discoveries into how–and when–this telomere-dedicated machine puts itself together.

Every time a cell divides, its entire genome must be duplicated. While this duplication is going on, Tucey discovered that telomerase sits poised as a “preassembly” complex, missing a critical molecular subunit. But when the genome has been fully duplicated, the missing subunit joins its companions to form a complete, fully active telomerase complex, at which point telomerase can replenish the ends of eroding chromosomes and ensure robust cell division.

Surprisingly, however, Tucey and Lundblad showed that immediately after the full telomerase complex has been assembled, it rapidly disassembles to form an inactive “disassembly” complex – essentially flipping the switch into the “off” position. They speculate that this disassembly pathway may provide a means of keeping telomerase at exceptionally low levels inside the cell. Although eroding telomeres in normal cells can contribute to the aging process, cancer cells, in contrast, rely on elevated telomerase levels to ensure unregulated cell growth. The “off” switch discovered by Tucey and Lundblad may help keep telomerase activity below this threshold.

Yale scientists have successfully used an arthritis medication to fully regrow the head and body hair of a almost totally hairless 25-year-old man.

Researchers administered the drug tofacitinib citrate to the unnamed patient, who suffered from the autoimmune baldness disease alopecia universalis.

Within eight months, the man had regrown scalp and facial hair he’d not had in seven years.

‘The results are exactly what we hoped for,’ said Brett A. King, M.D., senior author of the paper, published in the Journal of Investigative Dermatology. ‘This is a huge step forward in the treatment of patients with this condition.’

.Unbelievable: Yale University researchers correctly guessed that a rheumatoid arthritis drug called Xeljanz could successfully regrow hair in a patient with the autoimmune disease alopecia universalis, which causes hairlessness over the whole body. This 25-year-old took the drug and by the end of eight months had all the hair back on his head, body and face that he hadn’t had in years

.Huge success: The drug had successfully been used before on plaque psoriasis, which the 25-year-old Yale patient also exhibited, but had never been used to treat alopecia in humans

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The man was referred to Yale Dermatology in New Haven, Connecticut to deal with an autoimmune disease that coincided with his alopecia, plaque psoriasis, according to a department news release.

Believing both his ailments could be alleviated with the same drug, researchers administered tofacitinib, made by Pfizer under the brand name Xeljanz, which is already FDA approved for the autoimmune disease rheumatoid arthritis.

According to Science World Report, the drug had successfully been used to treat psoriasis in people and alopecia in mice.

But the results were nonetheless shocking.

Photos of the man show him go from totally bald on top of his head to sporting a lustrous mane of blond locks.

‘There are no good options for long-term treatment of alopecia universalis,’ said King. ‘The best available science suggested this might work, and it has.’

The patient took 10mg per day for two months followed by 15mg per day for another three months.

By the end, he’d completely regrown scalp hair, developed eyebrows, eyelashes and facial hair, armpit hair and other hair.

‘By eight months there was full regrowth of hair,’ said co-author Brittany G. Craiglow, M.D. ‘The patient has reported feeling no side effects, and we’ve seen no lab test abnormalities, either.’

According to King, scientists believe the drug works by turning off the immune attack on hair follicles.

The authors said the drug helps in some but not all instances of psoriasis.

Scientists in the Netherlands have moved a step closer to overriding one of Albert Einstein’s most famous objections to the implications of quantum mechanics, which he described as “spooky action at a distance.”

In a paper published on Thursday in the journal Science, physicists at the Kavli Institute of Nanoscience at the Delft University of Technology reported that they were able to reliably teleport information between two quantum bits separated by three meters, or about 10 feet.

Quantum teleportation is not the “Star Trek”-style movement of people or things; rather, it involves transferring so-called quantum information – in this case what is known as the spin state of an electron – from one place to another without moving the physical matter to which the information is attached.

Classical bits, the basic units of information in computing, can have only one of two values – either 0 or 1. But quantum bits, or qubits, can simultaneously describe many values. They hold out both the possibility of a new generation of faster computing systems and the ability to create completely secure communication networks.

. A forest of optical elements that was part of the quantum teleportation device used by the team of physicists in the Netherlands. Credit Hanson lab@TUDelft

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Moreover, the scientists are now closer to definitively proving Einstein wrong in his early disbelief in the notion of entanglement, in which particles separated by light-years can still appear to remain connected, with the state of one particle instantaneously affecting the state of another.

They report that they have achieved perfectly accurate teleportation of quantum information over short distances. They are now seeking to repeat their experiment over the distance of more than a kilometer. If they are able to repeatedly show that entanglement works at this distance, it will be a definitive demonstration of the entanglement phenomenon and quantum mechanical theory.

Succeeding at greater distances will offer an affirmative solution to a thought experiment known as Bell’s theorem, proposed in 1964 by the Irish physicist John Stewart Bell as a method for determining whether particles connected via quantum entanglement communicate information faster than the speed of light.

“There is a big race going on between five or six groups to prove Einstein wrong,” said Ronald Hanson, a physicist who leads the group at Delft. “There is one very big fish.”

In the past, scientists have made halting gains in teleporting quantum information, a feat that is achieved by forcing physically separated quantum bits into an entangled state.

Interactive Graphic
QUANTUM TELEPORTATION
Researchers teleported quantum information between two distant atoms for the first time in 2009.
Click on image below to open interactive graphic

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But reliability of quantum teleportation has been elusive. For example, in 2009, University of Maryland physicists demonstrated the transfer of quantum information, but only one of every 100 million attempts succeeded, meaning that transferring a single bit of quantum information required roughly 10 minutes.

In contrast, the scientists at Delft have achieved the ability “deterministically,” meaning they can now teleport the quantum state of two entangled electrons accurately 100 percent of the time.

They did so by producing qubits using electrons trapped in diamonds at extremely low temperatures. According to Dr. Hanson, the diamonds effectively create “miniprisons” in which the electrons were held. The researchers were able to establish a spin, or value, for electrons, and then read the value reliably.

In addition to the possibility of an impregnable quantum Internet, the research holds out the possibility of networks of quantum computers.

To date, practical quantum computers, which could solve certain classes of problems far more quickly than even the most powerful computers now in use, remain a distant goal. A functional quantum computer would need to entangle a large number of qubits and maintain that entangled state for relatively long periods, something that has so far not been achieved.

A distributed quantum network might also offer new forms of privacy, Dr. Hanson suggested. Such a network would make it possible for a remote user to perform a quantum calculation on a server, while at the same time making it impossible for the operator of the server to determine the nature of the calculation.

The study, published online in Nature Methods and conducted by a team led by Chinese stem-cell biologist Duanqing Pei, found that cells generated from human waste might someday be used to study disease and even in therapeutic treatments for neurodegenerative diseases.

Plus, there’s a potential added bonus to the discovery: Embryonic stem cells possess a high risk of developing tumors, which reportedly would not be an issue with cells taken from the urine samples.

The process works by transforming cells present in the urine into precursors of brain cells, known as neural progenitor cells. The study says the cells found in urine are a “much more accessible source” than cells found in skin and blood samples.

“This could definitely speed things up,” James Ellis, a medical geneticist at Toronto’s Hospital for Sick Children in Ontario, Canada, told Nature.